Skip to main content
Figure 4 | Journal of Neuroinflammation

Figure 4

From: Minocycline, a microglial inhibitor, blocks spinal CCL2-induced heat hyperalgesia and augmentation of glutamatergic transmission in substantia gelatinosa neurons

Figure 4

TNF-α antagonist WP9QY blocks CCL2-induced enhancement of excitatory synaptic transmission in substantia gelatinosa neurons and inhibits CCL2-induced heat hyperalgesia. (A) Intrathecal administration of CCL2 increased the frequency of spontaneous mEPSCs in a lamina II neuron. Intrathecal co-injection of WP9QY and CCL2 completely inhibited the CCL2-induced increase in the frequency of mEPSCs in a lamina II neuron. V H = -60 mV. (B) After co-administration with WP9QY, CCL2 failed to increase the frequency of mEPSCs in substantia gelatinosa neurons. Each bar shows mean ± standard error for 12 neurons from 6 rats. *P < 0.01 compared to control neurons. # P < 0.01 compared to CCL2-treated neurons. (C) Intrathecal injection of CCL2 (1 μg) decreased hind-paw withdrawal latency and caused thermal hyperalgesia. Intrathecal co-administration of WP9QY and CCL2 completely inhibited CCL-induced heat hyperalgesia. Each bar represents mean ± standard error for ten rats. *P < 0.01 compared to control rats. Con, control; mEPSC, miniature excitatory postsynaptic current.

Back to article page